INVITRO STUDIES OF MEGAKARYOCYTOPOIESIS IN THROMBOCYTOTIC DISORDERS OF MAN

  • 1 January 1983
    • journal article
    • research article
    • Vol. 61  (2) , 384-389
Abstract
Increased numbers of bone marrow megakaryocytes and thrombocytosis are frequently observed in patients with myeloproliferative disorders (MPD). Increased marrow megakaryocytes and thrombocytosis are also noted in a variety of inflammatory and neoplastic diseases leading to the phenomenon of reactive thrombocytosis (RT). The pathogenesis of this finding remains incompletely understood. The causative role of megakaryocyte colony-stimulating activity (Meg-CSA) in generating this phenomenon was investigated. The cloning efficiency of colony-forming units-megakaryocyte (CFU-M) and their responsiveness to an exogenous source of Meg-CSA in patients with these diseases were examined. Increased production of Meg-CSA is not responsible for the megakaryocyte hyperplasia and thrombocytosis noted in these patients. The intrinsic stem cell defect described in MPD appears to affect the CFU-M of these patients as well, resulting in an effective expansion of the CFU-M pool with consequent megakaryocyte hyperplasia and thrombocytosis. The CFU-M of patients with MPD remain responsive to an exogenous source of Meg-CSA, suggesting that this megakaryocyte hyperplasia may not be entirely autonomous of its effects. The CFU-M pool in RT is normal both in size and reponsiveness to Meg-CSA, suggesting that in these disorders, the stimulus leading to megakaryocyte hyperplasia and thrombocytosis is active at the post-CFU-M level of megakaryocyte differentiation.